Excess wound contraction and inadequate scar formation in the adult are characterized by collagen deposition resulting in numerous pathologic conditions such as intestinal adhesions and pressure ulcers, for which there are few therapeutic options. In contrast, fetal wounds heal with scarlessly and with a higher ratio of collagen type III to type 1a1 deposition than in adult wounds. Transforming growth factor beta (TGF-b) has been implicated to be an important mediator of wound healing and the TGF-b isoforms may have a role in both the transition from the fetal scarless wound to the adult scar-forming wound. This study aims at exploring the relationship between TGF-b and wound healing by determining if TGF-b1 and -b3 differentially regulate procollagen 1a1 and procollagen III gene expression in an in vitro model by using the same cell- surface receptor yet through different cell signaling pathways. [unreadable] [unreadable] [unreadable]